The mitochondrion is an organelle found in most eukaryotic cells. One of the major functions thereof is oxidative phosphorylation, through which energy derived from a metabolism of fuel materials such as glucose or fatty acid, etc. is converted into adenosine triphosphate (ATP). ATP is used in driving various energy-requiring biosynthesis processes and other metabolic activities. The mitochondrion includes its own DNA distinct from nuclear genomic DNA. The mitochondrial DNA is known as having a circular form and approximately 16,000 base pairs. Further, the mitochondrial DNA lacks its own repair mechanism unlike the nuclear DNA, and histones acting as DNA protectors, and thus is susceptible to mutations caused by intracellular or extracellular environments. Such mutations mostly exhibit an effect of inhibiting mitochondrial activity, whereas they may partly exhibit an effect of enhancing the same.
If the mitochondrial activity is inhibited by the mutations in the mitochondrial DNA, swelling caused by an abnormality of mitochondrial membrane potential, dysfunctions by oxidative stress by reactive oxygen species or free radicals, etc., dysfunctions by genetic factors, or dysfunction by defects in oxidative phosphorylation functions for energy production of mitochondria may occur, which are known as having potential to cause a metabolic disease, degenerative brain disease, liver dysfunction, muscle disease, immune disease, etc. In this regard, various preparations are being developed to treat such diseases caused by the inhibition of mitochondrial activity (Korean Patent No. 1048766, Korean Laid-open Patent Application Nos. 2005-0117313, 2013-0064761, 2014-0012456, etc.).
Meanwhile, when the mitochondrial DNA is mutated and the activity of mitochondria is promoted, intracellular ATP is excessively produced, and consequently cellular dysfunctions may occur, by which multiple diseases may be caused, such as various autoimmune diseases including rheumatoid arthritis, and various types of cancer. Various studies on diseases caused by the inhibition of mitochondrial activity are being conducted in terms of promoting the mitochondrial activity. Still, an appropriate activator to improve the inhibition of mitochondrial activity has not been developed. It is because, although various candidate materials have been discovered which exhibit mitochondrial function-promoting activity, they were unable to substantially promote mitochondrial function. Accordingly, necessity for developing a method to find such activators that can substantially promote the mitochondrial function emerged.